Contents
Academic literature on the topic 'Can Low Testosterone Cause ED?'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Can Low Testosterone Cause ED?.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Journal articles on the topic "Can Low Testosterone Cause ED?"
1
Singh, Santosh. "Aromatase Inhibitors in Erectile Dysfunction." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A755. http://dx.doi.org/10.1210/jendso/bvab048.1535.
Full textAbstract:
Abstract Hyperestrogenism may cause erectile dysfunction(ED) by impeding normal penile development,increasing venous vascular permeability and leakage(via VEGF) and by inhibiting testosterone(T)production. Estrogen excess can impair spermatogenesis and may increase the risk of estrogen-sensitive cancers(viz.breast cancer)[1,2]Weekly and biweekly letrozole(2.5 mg),an aromatase inhibitor,has been reported to normalize serum T in males with obesity related hypogonadism and poor sperm quality,respectively.[3,4]A 40-year old insulin requiring,normotensive,obese(BMI-26.9),diabetic(12 years duration) was evaluated for ED.T was 187 ng/dl and estradiol(E2) was 69 pg/ml(normal-11-44 pg/ml) with normal LH and prolactin levels. There was normalization of T(increased to 487 ng/dl) with 2.5 mg letrozole every 3 weeks. Another patient,55 year old male, insulin requiring,hypertensive,obese(BMI-28.8),diabetic(21 years duration) had normalization of T(401 ng/dl) with baseline low T(224.4 ng/dl) and normal E2(33 pg/ml) with T-E2 ratio of less than 10,with weekly 2.5 mg letrozole. There was one kg weight gain and 0.2 ng/ml increase in PSA in two years. These cases highlight the significance of estimating both T and E2 in the evaluation of ED. Moreover,it also highlights the efficacy and safety of weekly and even every 3-week 2.5 mg letrozole therapy. References: 1. .Schulster M,Bernie AM,Ramasamy R:The role of estradiol in male reproductive function.Asian Journal of Andrology,2016,18(3),435-440. 2. Goldfrank LR and Flomenbaum N:Goldfrank’s Toxicologic Emergencies,McGraw- Hill Professional,2006,p443. 3.Loves S,Ruinemans-Koerts,de Boer H:Letrozole once a week normalizes serum testosterone in obesity-related male hypogonadism. Eur J Endocrinol,2008,158,741-747.4. Singh SK:Aromatase inhibitors in male sex. Indian J Endocrinol Metab,2013,17,S259-261.
2
Saraheni, Saraheni, I. Dewa Putu Pramantara, and Herni Astuti. "Asupan zink dan magnesium makanan dengan disfungsi ereksi pada penderita sindrom metabolik." Jurnal Gizi Klinik Indonesia 10, no. 3 (January 30, 2014): 127. http://dx.doi.org/10.22146/ijcn.18861.
Full textAbstract:
Background: Metabolic syndrome (MetS) is a disease of disorder of lipid and nonlipid metabolism. The West of Scotland Coronary Prevention Study found that men with MetS had probability 3.7 dysfunctions of erection (ED) by using International Index of Erectile Function (IIEF). Patient with heart disease had the risk 2 times to get ED, hypertension was 1.5-2 times, DM was 3-4 times, depression was 2-3.5 times, testosterone deficiency syndrome (TDS) was 1.5-2 times, and high cholesterol was 4 times. The nutrient deficiency of zinc (Zn) and magnesium (Mg) was suspected being the main component which had a role in resisting a sexuality growth and maturation process.Objective: Knowing the correlation of Zn and Mg feeding with erection dysfunction in MetS person.Method: This study was observational analytic study, with case-control design in the patient aged 30-60 years old. The respondent in this study was people with MetS according to WHO criterion. There was 82 patient divided into two groups, consist of 41 cases of MetS and ED, 41 cases with the normal patient. The data collected by interview, laboratory assessment and anthropometric measurement. The data analysis using univariate, bivariate and multivariate analysis using multiple logistic regression.Results: There was significant correlation between Zn feeding and ED (OR=7.15; 95% Cl=1.47-34.71; p=0.007) and there was significant correlation between Mg feeding with ED (OR=3.34; 95% Cl=1.07-10.4; p=0.033). The end result of the multivariate analysis showed the risk variable to the ED event, that was Zn feeding with OR=15.41. If the intake of Zn accompanied with risk factors associated as a cause of ED, multivariate analysis showed HbA1c’s degree with OR=12.57; triglyceride (OR=10.47); blood pressure (OR=5.82); and abdominal obesity (OR=6.94). The result shows that these risk factors can aggravate or anticipate the onset of dysfunction erection beside low Zn intake.Conclusion: There was statistically significant correlation between Zn and Mg feeding with erection dysfunction in MetS patient.
3
Kirby, Michael, Geoffrey Hackett, and Sudarshan Ramachandran. "Testosterone and the Heart." European Cardiology Review 14, no. 2 (July 11, 2019): 103–10. http://dx.doi.org/10.15420/ecr.2019.13.1.
Full textAbstract:
The development of a subnormal level of testosterone (T) is not universal in ageing men, with 75% of men retaining normal levels. However, a substantial number of men do develop T deficiency (TD), with many of them carrying a portfolio of cardiovascular (CV) risk factors, including type 2 diabetes (T2D) and the metabolic syndrome. TD increases the risk of CV disease (CVD) and the risk of developing T2D and the metabolic syndrome. The key symptoms suggesting low T are sexual in nature, including erectile dysfunction (ED), loss of night-time erections and reduced libido. Many men with heart disease, if asked, admit to ED being present; a problem that is often compounded by drugs used to treat CVD. A large number of studies and meta-analyses have provided evidence of the link between TD and an increase in CVD and total mortality. Patients with chronic heart failure (CHF) who have TD have a poor prognosis and this is associated with more frequent admissions and increased mortality compared with those who do not have TD. Conversely, in men with symptoms and documented TD, T therapy has been shown to have beneficial effects, namely improvement in exercise capacity in patients with CHF, improvement of myocardial ischaemia and coronary artery disease. Reductions in BMI and waist circumference, and improvements in glycaemic control and lipid profiles, are observed in T-deficient men receiving T therapy. These effects might be expected to translate into benefits and there are more than 100 studies showing CV benefit or improved CV risk factors with T therapy. There are flawed retrospective and prescribing data studies that have suggested increased mortality in treated men, which has led to regulatory warnings, and one placebo-controlled study demonstrating an increase in coronary artery non-calcified and total plaque volumes in men treated with T, which is open for debate. Men with ED and TD who fail to respond to phosphodiesterase type 5 (PDE5) inhibitors can be salvaged by treating the TD. There are data to suggest that T and PDE5 inhibitors may act synergistically to reduce CV risk.
4
Otunctemur, Alper, Emin Ozbek, Suleyman Sami Cakir, Murat Dursun, Emre Can Polat, Levent Ozcan, and Huseyin Besiroglu. "Urolithiasis is associated with low serum testosterone levels in men." Archivio Italiano di Urologia e Andrologia 87, no. 1 (March 31, 2015): 83. http://dx.doi.org/10.4081/aiua.2015.1.83.
Full textAbstract:
Objective: To evaluate the relationship among urolithiasis, metabolic syndrome (MetS) and serum testosterone (T) level in men. Material and Methods: 513 men older than 18 years were enrolled in this study: 313 of the subjects had a history of stones (group 1) and 200 had no history of stones (controls, group 2). Early morning T levels were recorded and anthropometric measurements were invastigated to evaluate MetS. Analyses were completed using chi-square tests. Result: Serum T level was lower in stone forming patients than coltrol subjects and 161 (%51.4) men in group 1 and 92 (%46) men in group 2 were diagnosed with metabolic syndrome. T level was found lower limit (< 285 ng/dl) in the MetS and urolithiasis group (p 0.002, OR 2.71). Conclusions: We found low testosterone levels in the patients with stone disease and prevalance of the MetS in men with urolithiasis was higher than in men without stone disease. Our findings show that levels of testosterone had no effect on stone formation, but the factors that cause stone formation can have an effect on the level of testosterone.
5
Nicholson, H. D., R. T. S. Worley, H. M. Charlton, and B. T. Pickering. "LH and testosterone cause the development of seminiferous tubule contractile activity and the appearance of testicular oxytocin in hypogonadal mice." Journal of Endocrinology 110, no. 1 (July 1986): 159–67. http://dx.doi.org/10.1677/joe.0.1100159.
Full textAbstract:
ABSTRACT Immunoreactive oxytocin is present in the testis and it has been shown that this hormone increases the contractility of seminiferous tubules. We have investigated the relationship between testicular oxytocin, tubular movements and the effects of LH and testosterone using, as a model, the hypogonadal (hpg/hpg) mouse, which is deficient in hypothalamic LH-releasing hormone (LHRH). Whilst both testicular oxytocin and seminiferous tubule movements, resembling those seen in the rat, can be found in normal adult mice, neither can be found in hypogonadal mice. After 2 weeks of treatment with LH (200 ng to 100 μg daily) low levels of testicular oxytocin and tubular movements were observed. Treatment with large doses of testosterone for 2–12 weeks led to higher concentrations of testicular oxytocin and tubular movements resembling those seen in the normal adult mouse. The results support the evidence that testicular oxytocin modulates seminiferous tubule movements. We suggest that testosterone may play a part in the accumulation of oxytocin in the testis. J. Endocr. (1986) 110, 159–167
6
Munshi, Lubna Bashir, Yumiko Tsushima, Kwan Cheng, and Maria Brito. "Megestrol Acetate-Induced Symptomatic Hypogonadism in a Male Patient." Case Reports in Endocrinology 2018 (July 18, 2018): 1–3. http://dx.doi.org/10.1155/2018/7048610.
Full textAbstract:
The hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-gonadal (HPG) axis are very sensitive and can be affected by external factors like stress, starvation, and medication. Medication-induced suppression of these axes can cause adrenal insufficiency (AI) and hypogonadism. Exogenous glucocorticoid use is the most common cause of iatrogenic AI. Our aim is to bring attention to another broadly prescribed medication, megestrol acetate (MA), as the cause of suppression of both these axes. We report a case of symptomatic hypogonadism and asymptomatic AI in a male patient secondary to MA. The patient presented with decrease in testicular size and erectile dysfunction. His total testosterone and morning cortisol levels were low, but FH, LH, and TSH were normal. His pituitary MRI was unremarkable. Upon discontinuation of MA, the patient’s testosterone and cortisol levels normalized and his symptoms resolved. Hypogonadism and AI are known adverse effects of MA, but symptomatic hypogonadism as the primary manifestation has only been reported once in previous literature. Prolonged hypogonadism can lead to sarcopenia, depression, and osteoporosis, while asymptomatic AI carries the risk of becoming overt AI. Thus, heightened awareness of the impact of MA on both these axes is necessary.
7
Crook, David. "Androgen therapy for ageing men: the implications for arterial disease." British Menopause Society Journal 8, no. 2 (June 1, 2002): 69–71. http://dx.doi.org/10.1258/136218002100321686.
Full textAbstract:
Steroid hormones such as oestradiol and testosterone have long been viewed as a key to long-term health. Although men do not undergo the precipitous fall in endogenous steroid hormone levels characteristic of the menopause, there is substantial interest in the therapeutic potential of low dose androgen therapies to maintain mental, skeletal and other aspects of health. Testosterone and other androgens seem to conform to the "clutch pedal" theory of hormone action. In terms of atherosclerosis, if plasma androgen levels are too low they may cause disease, but, if they are too high, atherosclerosis may also become a problem. Thus, the rationale for the use of low doses of androgens in ageing males is becoming compelling. Studies of arterial disease surrogates, such as plasma protein levels, may help optimise these therapies but the final answer on disease can only come from formal placebo-controlled trials of clinical endpoints.
8
Zarei, Ali, Saeed Changizi Ashtiyani, and Gholam Hassan Vaezi. "A study on the effects of the hydroalcholic extract of the aerial parts of Alhagi camelorum on prolactin and pituitary-gonadal activity in rats with hypercholesterolemia." Archivio Italiano di Urologia e Andrologia 86, no. 3 (September 30, 2014): 188. http://dx.doi.org/10.4081/aiua.2014.3.188.
Full textAbstract:
Background: Although endocrine disorders are not a common cause of infertility, in some cases, testing thyroid function, and hypothalamus - pituitary - gonadal axis can determine the cause of infertility. We aimed to investigate the effect of the aerial parts of Alhagi camelorum extract on prolactin, cortisol and pituitary - gonadal axis activities in rats with hypercholesterolemia. Materials and methods: In this study, 35 male wistar rats in 5 groups (n = 7) were assigned as: control group with normal diet, the sham group with fat diet and three experimental groups of hypercholesterolaemic animals which received Alhagi camelorum extract at a minimum dose of 100 mg/kg, average dose of 200 ml/kg and maximum dose of 300 mg/kg over a period of 21 days. At the end of the period, blood samples were collected from all groups and blood factors were then measured and analyzed. Results: In the sham group compared to the control, cholesterol levels increased and FSH levels decreased, whereas cholesterol levels reduced in the experimental groups. Alhagi camelorum extract also reduced testosterone level and increased prolactin and gonadotropins. Conclusion: Alhagi camelorum extract at low and average doses reduced cortisol, testosterone and cholesterol and increased gonadotropins. So it can cause reproductive disorders in male rats. The extract at maximum dose can increase cortisol and prolactin. As these two hormones work together to produce milk, this plant can help to boost breastfeeding.
9
Mittal, Ashima, Sanat Mishra, Karamvir Yadav, and Rajesh Rajput. "Uncontrolled diabetes as a rare presenting cause of pituitary apoplexy." BMJ Case Reports 12, no. 2 (February 2019): bcr—2018–228161. http://dx.doi.org/10.1136/bcr-2018-228161.
Full textAbstract:
Pituitary apoplexy is a rare endocrine emergency. The extent to which hyperglycaemia is a contributory risk factor in the precipitation of pituitary apoplexy is not known. A 38-year-old man with poorly controlled diabetes presented to the emergency department with sudden onset of nausea and headache with drooping of his right eyelid for about 4 days. On physical examination, he had orthostatic hypotension, ptosis of the right eye, lateral and downward positioning of the eye and absent pupillary reflex. Visual field testing of the left eye revealed superolateral quadrantanopia. MRI of the brain showed pituitary macroadenoma with necrosis. Investigations showed hyperglycaemia, decreased T3, T4 with normal Thyroid stimulating hormone (TSH), low serum Leutinizing hormone (LH), Follicle stimulating hormone (FSH), testosterone and low normal serum prolactin levels. About 21% of non-functioning pituitary adenomas present with apoplexy as was seen in our patient. It is likely that his uncontrolled diabetes precipitated this episode of apoplexy as hyperosmolarity and dehydration, caused by hyperglycaemia can lead to changed pituitary microvascular environment increasing the risk of pituitary infarction.
10
Nandu, Nitish Singh, Wafa Dawahir, Swetha Paduri, Janice L. Gilden, and Dennis L. Citrin. "Can Long-Standing GnRH Therapy Cause a Pituitary Prolactinoma?" Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A574—A575. http://dx.doi.org/10.1210/jendso/bvab048.1172.
Full textAbstract:
Abstract Background: Pituitary adenoma (PA) is the most common cause of sellar masses and accounts for about 10% of all intracranial tumors. Several physiological, pathological, drugs, and rare causes like hypothyroidism can cause PA. We describe a case of long-standing treatment with GnRH analogues possibly contributing to development of PA. Clinical Case: An 86-year-old man with a history of prostate cancer (PC) treated with medical therapy, presented to the hospital with progressively worsening loss of vision in his right eye associated with low-grade headaches over the past few years. Fifteen years prior to presentation, the patient was diagnosed with Gleason 6 (3 + 3) localized PC. He had refused surgical intervention and hence was treated with flutamide, then leuprolide. Labs were significant for an elevated prolactin 34.2 ng/mL [n= 2.5 -17.4], low LH 0.7 mIU/mL [n=1.2-10.6], with normal FSH, TSH, ACTH, IGF, Cortisol, and PTH. CT head and MRI brain identified a 2.7cm x 2.6.3 cm X 1.7 cm mass in the suprasellar region involving the left cavernous sinus and right optic chiasm. These findings were consistent with a diagnosis of Prolactinoma. Patient refused surgery and hence was started on bromocriptine. The findings were suspected to be secondary to long-standing GnRH agonist therapy, and leuprolide was discontinued. DEXA scan confirmed osteoporosis with a T score of --2.5, which was treated with denosumab. Subsequently his vision improved. The patient continues to follow with endocrinology for the management of osteoporosis and prolactinoma. Conclusion: Primary hypothyroidism predisposes to PA due to loss of thyroxine feedback inhibition to hypothalamus with overproduction of TRH with hyperplasia of lactotrophs. We speculate that constant stimulation of the pituitary by GnRH analogues can also lead to enlargement of the anterior pituitary in a similar fashion, and can lead to the development of prolactinoma. LHRH agonists such as Leuprolide, as palliative treatment for advanced prostate cancer, causes desensitization of the anterior pituitary and decreases the production of LH and FSH, which ultimately leads to decreased testosterone in males. Although not standard of care for treatment of locally advance tumors, medical therapy was chosen in this patient’s case due to refusal of surgical intervention. He then developed a clinically significant pituitary adenoma years after the therapy. We suggest that constant stimulation of the pituitary by GnRH analogues can lead to enlargement of the anterior pituitary in a similar fashion, resulting in the development of the prolactinoma. Reference(1) Du J, Ji H, Jin J, Gao S, Yan X, Hu S. Pituitary adenoma secondary to primary hypothyroidism: Two case reports. Medicine (Baltimore). 2020;99(8). https://journals.lww.com/md-journal/Fulltext/2020/02210/Pituitary_adenoma_secondary_to_primary.47.aspx
Book chapters on the topic "Can Low Testosterone Cause ED?"
1
Lambrecht, Thijs, and Wouter Ryckbosch. "Economic inequality in the rural Southern Low Countries during the Fifteenth century: sources, data and reflection." In Disuguaglianza economica nelle società preindustriali: cause ed effetti / Economic inequality in pre-industrial societies: causes and effect, 205–29. Florence: Firenze University Press, 2020. http://dx.doi.org/10.36253/978-88-5518-053-5.16.
Full textAbstract:
This chapter seeks to explore local and regional variation in levels of inequality in different types of rural localities and regions within the late medieval County of Flanders. Our research indicates that fiscal sources for the County of Flanders can produce reliable data on the distribution of income during the late medieval period. The analysis of these data shows that important local and regional differences can be observed in the distribution of rural income. To a large extent, these local variations can be explained by differences in access to local economic resources. Our results, however, also indicate that substantial regional differences in access to rural resources can produce similar income distributions.
2
Hathiramani, Sumitha S., and Hans K. Ghayee. "Assessment of Endocrine Function." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0007.
Full textAbstract:
This chapter describes the various methods used for quantifying concentrations of circulating hormones and thus assessing endocrine function. The paradigm of feedback regulation (for example, of the hypothalamic-pituitary-target gland axis) is central to this assessment of endocrine status. Any disruption in such an axis can cause alterations in trophic and target hormone pairs. High concentration of a target gland hormone coupled with low concentration of the corresponding trophic hormone (e.g., pituitary hormone) suggests autonomous secretion by the target endocrine organ, as is typical in primary hyperthyroidism, e.g., high thyroxine (T4), suppressed thyroid stimulating hormone (TSH). Elevated concentrations of both members of a hormone pair usually indicate autonomous secretion of the trophic hormone, either from the normal site or from a tumor in an “ectopic” (extraglandular) location. For example, excess cortisol production driven by a high plasma adrenocorticotropic hormone (ACTH) level may be due to the secretion of pituitary ACTH or secretion of ACTH by lung tumors. Alternatively, the combined elevation of trophic and target endocrine gland hormones can result from resistance to the action of the target endocrine gland hormone e.g., elevated luteinizing hormone (LH) and testosterone in androgen resistance. Autonomous hypersecretion of the trophic hormone typically results in clinical evidence of target gland hormone excess, whereas resistance to the target gland hormone leads to manifestations of hormone deficiency. Hormones circulating in the plasma were first detected by in vivo bioassays, in which plasma or extracts of plasma were injected into animals and biological responses were measured. Unfortunately, most in vivo bioassays lack the precision, sensitivity, and specificity required to measure the low concentrations of many hormones in plasma, and the assays are cumbersome and impractical for routine use in clinical chemistry laboratories. Great progress in measuring plasma hormone concentrations came with the development of radioimmunoassays (RIAs) in the late 1950s. An unknown concentration of hormone in plasma is estimated by allowing competition with a labeled hormone or analog for specific binding sites on an antibody.